Objective: To investigate the effect of cerebrolysin (CBL) on motor impairment, neuroinflammation, oxidative stress, and neurotransmitter profile in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson’s disease (PD) in zebrafish.
Methods: In the current study, zebrafish were treated with CBL at doses of 1.25, 2.5, and 5 mL/kg body weight for 7 consecutive days. MPTP (20 mg/kg body weight) was administered on alternative days-lst, 3rd, 5th, and 7th. On day 7, zebrafish were sacrificed, and their brains were isolated for biochemical, neurochemical, histopathological, IHC, and neurotransmitter analysis.
Results: The treatment with CBL significantly increased total distance traveled and the number of entries in the top zone, which was impaired by MPTP. CBL treatment significantly restored the level of glutathione, superoxide dismutase, and catalase while reducing malondialdehyde level. It also reduced the level of pro-inflammatory mediators interleukin-1β, interleukin-6, and tumor necrosis factor-α in the MPTP-induced PD in the zebrafish model. In histopathological evaluation, pyknotic cells and signs of inflammation were significantly reduced in CBL-treated groups. A significant dose-dependent reduction in glutamate, along with elevations in dopamine, gamma-aminobutyric acid, serotonin, and noradrenaline, was observed in zebrafish treated with CBL. An immunohistochemistry analysis demonstrated that Akt was phosphorylated promptly by CBL, which was downregulated in MPTP-induced PD in zebrafish.
Conclusions: These findings suggest that CBL exerts a neuroprotective effect through activation of Akt and may hold therapeutic potential for the treatment of this devastating neurological condition.
Objective: To investigate whether nacre extract improves insulin sensitivity, brain glucose metabolism, and cognitive function in diabetic mice.
Methods: Diabetic KK-Ay mice (n=5/group) were fed a standard diet or diets supplemented with nacre extract (125 or 250 mg/kg) for 13 weeks. Metabolic status was assessed by measuring fasting glucose and insulin levels, HOMA-IR, glucose tolerance, and insulin tolerance. The expression of IRS-1, IRS-2, and GLUT4 in the brain was analyzed by qPCR, Western blotting, and immunohistochemistry. Cognitive and anxiety-like behaviors were evaluated using the Y-maze, novel object recognition, Barnes maze, and open field tests.
Results: Nacre extract significantly reduced fasting glucose and insulin levels, improved HOMA-IR, and enhanced glucose and insulin tolerance (P<0.05) in diabetic mice. It also restored GLUT4 expression and significantly upregulated SIRT1 and BDNF. Behavioral assessments showed significant improvements in memory and reduced anxiety-like behaviors.
Conclusions: Nacre extract enhances insulin sensitivity, improves brain glucose metabolism, and alleviates cognitive and emotional dysfunction in diabetic mice. Further studies are warranted to verify the exact molecular mechanisms and efficacy of nacre extract in diabetes-associated metabolic and neurocognitive dysfunction.
Objective: To assess the protective effects of Panax ginseng (PG) against copper sulfate (CuSO4)-induced kidney toxicity in rats.
Methods: The rats were randomly allocated into four groups: control, CuSO4, PG, and PG+CuSO4. The experiment continued for 14 days, during which CuSO4 was provided at a dosage of 100 mg/kg body weight per day and PG at 300 mg/kg body weight by oral gavage per day. Upon completion of the experiment, kidney sections were used for histological and histomorphometric analyses. The histochemical method was applied to ascertain the density of the glomerular mesangial matrix. The expressions of vascular endothelial growth factor (VEGF) and caspase-3 were examined using immunohistochemistry. The levels of malondialdehyde and glutathione, along with the activity of superoxide dismutase and catalase in the kidney, were measured.
Results: PG treatment exhibited a marked protective effect against CuSO4-induced renal damage, as evidenced by improved histopathological lesions, significantly reduced glomerular mesangial matrix density, VEGF in distal tubules, caspase-3 expression, and malondialdehyde levels in renal tissue, as well as enhanced superoxide dismutase and catalase activities.
Conclusions: PG treatment ameliorates CuSO4-induced kidney injury in rats. Further studies are warranted to verify its efficacy and elucidate the underlying mechanism of its nephroprotective action.
Objective: To investigate the mechanisms by which unripe papaya extract (UCP) protects skin keratinocytes from UVB-induced inflammation and apoptosis.
Methods: High-performance liquid chromatography was used to identify the phytochemical composition of UCP. The free radical scavenging capacity of UCP was assessed against O2.-, and H2O2. HaCaT cells were pre-treated with varying concentrations of UCP and exposed to 40 mJ/cm2 UVB radiation. Cell viability, reactive oxygen species (ROS) levels, apoptotic markers, and inflammatory mediators were evaluated using standard biochemical assays and molecular techniques.
Results: UCP treatment significantly improved cell viability and reduced intracellular ROS and the release of O2.- and H2O2. UCP also inhibited apoptosis, as evidenced by reduced cytochrome c release and suppression of Akt phosphorylation. Additionally, UCP exhibited anti-inflammatory effects by downregulating COX-2 expression, suppressing PGE2 release, and inhibiting c-Jun and NF-κB signaling pathways.
Conclusions: UCP effectively protects skin keratinocytes from UVB-induced oxidative stress, inflammation, and apoptosis. These findings support its potential as a natural therapeutic agent for preventing UV-related skin damage. However, in vivo studies are warranted to confirm its efficacy.